Isorhamnetin attenuates liver fibrosis by inhibiting TGF-β/Smad signaling and relieving oxidative stress
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- 作者：Ji Hye Yanga ; 1 ; Sang Chan Kimb ; 1 ; Kyu Min Kima ; Chang Ho Janga ; Sam Seok Choa ; Seung Jung Kima ; Sae Kwang Kub ; Il Je Chob ; Sung Hwan Kia ; shki@chosun.ac.kr" class="auth_mail" title="E-mail the corresponding author
- 关键词：ALT ; alanine transaminase ; ARE ; antioxidant response element ; AST ; aspartate transaminase ; COL1A1 ; collagen 1A1 ; ECM ; extracellular matrix ; GCL ; glutamate-cysteine ligase ; GSH ; glutathione ; 4-HNE ; 4-hydroxynonenal ; HO-1 ; heme oxygenase-1 ; HSCs ; hepatic stellate cells ; Nrf2 ; NF-E2-related factor 2 ; PAI-1 ; plasminogen activator inhibitor-1 ; PPARγ ; peroxisome proliferator-activated receptor gamma ; SBEs ; Smad binding elements ; SMA ; smooth muscle actin ; TAK1 ; TGF-β-activated kinase 1 ; TGF ; transformi
- 刊名：European Journal of Pharmacology
- 出版年：2016
- 出版时间：15 July 2016
- 年：2016
- 卷：783
- 期：Complete
- 页码：92-102
- 全文大小：1858 K
文摘
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We investigated the ability of isorhamnetin protect against hepatic fibrosis.
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Isorhamnetin inhibited TGF-β1-induced fibrogenic gene expression in HSCs.
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Isorhamnetin blocked TGF-β1-induced ROS production via Nrf2 activation.
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Isorhamnetin significantly prevented CCl4-induced liver fibrosis in vivo.
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Isorhamnetin may be a promising therapeutics for the liver fibrosis.